Figure 1.

GK decreased ER stress‐induced cell death and apoptosis in NRCMs. NRCMs were pretreated with or without GK at the indicated concentrations (5, 10 and 20 μM respectively) for 12 h followed by treatment with ER stressors (tunicamycin, Tm, 2.5 μg·mL⁻¹, 24 h; thapsigargin, Tg, 300 nM, 24 h; H₂O₂, 100 μM, 4 h). (A–C) ER stressor‐induced cell death was measured by the LDH method. (D, E) Apoptosis was detected by the TUNEL assay (scale bar, 40 μm), and the TUNEL‐positive cells were quantified. (F–L) Western blot analysis showed that tunicamycin‐induced CHOP, cleaved caspase 3, cleaved PARP and cytosolic cytochrome c were suppressed by pretreatment with GK. However, tunicamycin‐suppressed Bcl‐2 and mitochondrial cytochrome c were increased by pretreatment with GK. COX4 and GAPDH, which are exclusively expressed in the mitochondria and cytosol, respectively, were used as controls for loading and fractionation. Data are presented as means ± SEM (n = 5); *P < 0.05. Cyt c, cytochrome c; mito, mitochondrial.